PANCREATIC β-CELL FUNCTION IN THE FETAL FOAL AND MARE

1980 ◽  
Vol 87 (2) ◽  
pp. 293-301 ◽  
Author(s):  
ABIGAIL L. FOWDEN ◽  
R. J. BARNES ◽  
R. S. COMLINE ◽  
MARIAN SILVER
Keyword(s):  
Gestational Age ◽  
Glucose Concentration ◽  
Cell Function ◽  
Insulin Concentration ◽  
Β Cell ◽  
Exogenous Glucose ◽  
Β Cell Function ◽  
The Mean ◽  
Mean Glucose ◽  
Mean Concentration

Insulin secretion and the factors influencing β-cell function were investigated in the chronically catheterized fetal foal and mare during the second half of gestation. The response of the fetal β cells to exogenous glucose was also examined. The mean concentration of insulin in the fetal foal was 7·5 ± 0·5 (s.e.m.) μu./ml (n = 20) which was significantly less than the corresponding maternal value of 49·0 ± 5·0μu./ml (n = 20, P<0·01). The insulin concentration in non-pregnant horses was 24·5 ± 1·5 μu./ml (n = 5) which was significantly less than the value in the pregnant animals (P<0·01). However, there was no significant difference in the mean glucose concentration between the groups of adult animals. The insulin concentration was related to the endogenous glucose level in both adult and fetal horses. Wide variation in the maternal insulin concentration was observed above a glucose concentration of about 5·0 mmol/l. The mean concentration of insulin in pregnant mares decreased with increasing gestational age while the mean glucose concentration remained unaltered throughout the second half of gestation. There was no change in the basal concentrations of insulin or glucose in the fetus with gestational age although the fetal β-cell response to exogenous glucose appeared to increase with increasing fetal age after 270 days of gestation (term 330 days). There was a significant arterio-venous difference in the concentration of insulin across the gravid uterus in the mare when the arterial insulin level was greater than 30 μu./ml. Below this value, there was no consistent uptake of insulin by the uterus. The observations are discussed in relation to the regulation of insulin release in utero and the effects of pregnancy on maternal β-cell function.

Impact of lack of suppression of glucagon on glucose tolerance in humans

1999 ◽  
Vol 277 (2) ◽  
pp. E283-E290 ◽  
Author(s):  
Pankaj Shah ◽  
Ananda Basu ◽  
Rita Basu ◽  
Robert Rizza
Keyword(s):  
Insulin Secretion ◽  
Glucose Concentration ◽  
Cell Function ◽  
Hormone Secretion ◽  
Glucose Production ◽  
Glucagon Secretion ◽  
Β Cell ◽  
Β Cell Function ◽  
Glucagon Suppression

People with type 2 diabetes have defects in both α- and β-cell function. To determine whether lack of suppression of glucagon causes hyperglycemia when insulin secretion is impaired but not when insulin secretion is intact, twenty nondiabetic subjects were studied on two occasions. On both occasions, a “prandial” glucose infusion was given over 5 h while endogenous hormone secretion was inhibited. Insulin was infused so as to mimic either a nondiabetic ( n = 10) or diabetic ( n = 10) postprandial profile. Glucagon was infused at a rate of 1.25 ng ⋅ kg−1 ⋅ min−1, beginning either at time zero to prevent a fall in glucagon (nonsuppressed study day) or at 2 h to create a transient fall in glucagon (suppressed study day). During the “diabetic” insulin profile, lack of glucagon suppression resulted in a marked increase ( P < 0.002) in both the peak glucose concentration (11.9 ± 0.4 vs. 8.9 ± 0.4 mmol/l) and the area above basal of glucose (927 ± 77 vs. 546 ± 112 mmol ⋅ l−1 ⋅ 6 h) because of impaired ( P < 0.001) suppression of glucose production. In contrast, during the “nondiabetic” insulin profile, lack of suppression of glucagon resulted in only a slight increase ( P< 0.02) in the peak glucose concentration (9.1 ± 0.4 vs. 8.4 ± 0.3 mmol/l) and the area above basal of glucose (654 ± 146 vs. 488 ± 118 mmol ⋅ l−1 ⋅ 6 h). Of interest, when glucagon was suppressed, glucose concentrations differed only minimally during the nondiabetic and diabetic insulin profiles. These data indicate that lack of suppression of glucagon can cause substantial hyperglycemia when insulin availability is limited, therefore implying that inhibitors of glucagon secretion and/or glucagon action are likely to be useful therapeutic agents in such individuals.

scholarly journals Dietary glycemic load, glycemic index, and refined grains intake are associated with reduced β-cell function in prediabetic Japanese migrants

2009 ◽  
Vol 53 (4) ◽  
pp. 429-434 ◽  
Author(s):  
Daniela Saes Sartorelli ◽  
Laércio Joel Franco ◽  
Renata Damião ◽  
Suely Gimeno ◽  
Marly Augusto Cardoso ◽  
...  
Keyword(s):  
Glycemic Index ◽  
Cell Function ◽  
Glycemic Load ◽  
Inverse Association ◽  
Dietary Intakes ◽  
Β Cell ◽  
Refined Grains ◽  
Dietary Glycemic Load ◽  
Β Cell Function ◽  
The Mean

OBJECTIVE: To investigate the association between carbohydrate intakes and β-cell function (HOMA-β) in Japanese-Brazilians with impaired glucose tolerance (IGT). METHODS: Dietary intakes were assessed by a validated food frequency questionnaire in a cross-sectional survey carried out in 2000. The associations between diet and HOMA-β were verified in 270 newly diagnosed IGT in multiple linear regression models. RESULTS: The mean (SD) age was 58 (11) years and the mean HOMA-β was 65 (47). The glycemic load was inversely associated with HOMA-β, β1 -0.140 (95%CI = -1.044; -0.078), p = 0.023. The inverse association was also observed for refined grains intakes: -0.186 (95%CI = -0.4862; -0.058), p = 0.012. After adjustments for body mass index, the glycemic index was inversely associated with HOMA-β: -0.1246 (95%CI = -2.2482, -0.0257), p < 0.001. CONCLUSIONS: These data suggested that dietary glycemic load, glycemic index, and refined grains intakes are associated with reduced β-cell function, and the quality of dietary carbohydrates may be relevant for maintaining β-cell function among individuals with IGT.

Large birth size, infancy growth pattern, insulin resistance and β-cell function

2021 ◽  
Author(s):  
Rong Huang ◽  
Yu Dong ◽  
Anne Monique Nuyt ◽  
Emile Levy ◽  
Shu-Qin Wei ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Gestational Age ◽  
Growth Pattern ◽  
Beta Cell Function ◽  
Cell Function ◽  
Birth Size ◽  
Model Assessment ◽  
Β Cell ◽  
Β Cell Function

Objective: Large birth size programs an elevated risk of type 2 diabetes in adulthood, but data are absent concerning glucose metabolic health impact in infancy. We sought to determine whether large birth size is associated with insulin resistance and β-cell function in infancy, and evaluate the determinants. Design and Participants: In the Canadian 3D birth cohort, we conducted a nested matched (1:2) study of 70 large-for-gestational-age (LGA, birth weight >90th percentile) and 140 optimal-for-gestational-age (OGA, 25th-75th percentiles) control infants. The primary outcomes were homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-β) at age 2-years. Results: HOMA-IR and HOMA-β were similar in LGA and OGA infants. Adjusting for maternal and infant characteristics, decelerated growth in length during early infancy (0-3 months) was associated a 25.8% decrease (95% confidence intervals 6.7-41.0%) in HOMA-β. During mid-infancy (3-12 months), accelerated growth in weight was associated with a 25.5% (0.35-56.9%) increase in HOMA-IR, in length with a 69.3% increase (31.4-118.0%) in HOMA-IR and a 24.5% (0.52-54.3%) increase in HOMA-β. Decelerated growth in length during late infancy (1-2 years) was associated with a 28.4% (9.5-43.4%) decrease in HOMA-IR and a 21.2% (3.9-35.4%) decrease in HOMA-β. Female sex was associated with higher HOMA-β, Caucasian ethnicity with lower HOMA-IR, and maternal smoking with lower HOMA-β. Conclusions: The study is the first to demonstrate that large birth size is not associated with insulin resistance and β-cell function in infancy, but infancy growth pattern matters. Decelerated infancy growth may be detrimental to beta-cell function.

scholarly journals A higher-carbohydrate, lower-fat diet reduces fasting glucose concentration and improves β-cell function in individuals with impaired fasting glucose

Metabolism ◽  
2012 ◽  
Vol 61 (3) ◽  
pp. 358-365 ◽  
Author(s):  
Barbara A. Gower ◽  
Laura Lee Goree ◽  
Paula C. Chandler-Laney ◽  
Amy C. Ellis ◽  
Krista Casazza ◽  
...  
Keyword(s):  
Impaired Fasting Glucose ◽  
Glucose Concentration ◽  
Cell Function ◽  
Fasting Glucose ◽  
Β Cell ◽  
Β Cell Function

scholarly journals Longitudinal Changes in Insulin Sensitivity and Body Composition of Small-For-Gestational-Age Adolescents after Cessation of Growth Hormone Treatment

2008 ◽  
Vol 93 (9) ◽  
pp. 3449-3454 ◽  
Author(s):  
Ruben H. Willemsen ◽  
Sten P. Willemsen ◽  
Anita C. S. Hokken-Koelega
Keyword(s):  
Body Composition ◽  
Gestational Age ◽  
Cell Function ◽  
Insulin Response ◽  
Fat Distribution ◽  
Β Cell ◽  
Gh Treatment ◽  
Glucose Effectiveness ◽  
Β Cell Function

Context: GH treatment reduces insulin sensitivity (Si). For small-for-gestational-age (SGA) subjects, who might have an increased risk to develop cardiovascular disease and type 2 diabetes, it is still uncertain how Si, β-cell function, and body composition change over time after stopping GH treatment. Objective: Our objective was to investigate longitudinal changes in Si, β-cell function, and body composition after cessation of long-term GH treatment. Design and Patients: We conducted a longitudinal study that included 48 SGA adolescents studied at adult height, while still on GH, and 6 months after GH stop and compared them with 38 appropriate-for-gestational-age (AGA) controls at both time points. Outcome Measure: We took paired measurements of Si and β-cell function, assessed by frequently sampled iv glucose tolerance tests with tolbutamide, and body composition, measured by dual-energy x-ray absorptiometry. Results: After stopping GH, Si (P = 0.006), glucose effectiveness (Sg; P = 0.009) and β-cell function (disposition index; P = 0.024) increased, whereas insulin secretion (acute insulin response; not significant) decreased. Fat percentage increased (P &lt; 0.0005), and lean body mass decreased (P &lt; 0.0005), but fat distribution remained unaltered, and body composition remained within the normal range. Compared with AGA controls, Si was lower during GH and became similar after GH stop, acute insulin response was higher at both time points, and glucose effectiveness and disposition index became higher. Conclusions: The GH-induced lower Si in SGA adolescents increases after stopping long-term GH treatment and becomes similar to that of AGA controls. Discontinuation of GH treatment is, however, also associated with an increase in percent body fat and with a decrease in lean body mass, without changes in fat distribution.

Metabolism and β-cell function of rat pancreatic islets exposed to human interleukin-1β in the presence of a high glucose concentration

1990 ◽  
Vol 26 (3) ◽  
pp. 245-251 ◽  
Author(s):  
Stellan Sandler ◽  
Klaus Bendtzen ◽  
Décio L. Eizirik ◽  
Eva Strandell ◽  
Michael Welsh ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
High Glucose ◽  
Glucose Concentration ◽  
Cell Function ◽  
Interleukin 1Β ◽  
High Glucose Concentration ◽  
Β Cell ◽  
Rat Pancreatic Islets ◽  
Β Cell Function

scholarly journals Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic β-cells

2005 ◽  
Vol 152 (1) ◽  
pp. 103-112 ◽  
Author(s):  
Steen B Haugaard ◽  
Ove Andersen ◽  
Flemming Dela ◽  
Jens Juul Holst ◽  
Heidi Storgaard ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Cell Function ◽  
Glucose Disposal ◽  
Β Cell ◽  
Intravenous Glucose ◽  
Glucose And Lipid Metabolism ◽  
Exogenous Glucose ◽  
Immunodeficiency Virus ◽  
Β Cell Function ◽  
Glucose Storage

Objectives: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and β-cell function in lipodystrophic HIV-infected patients. Methods: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naïve to antiretroviral therapy (NAÏVE) respectively). β-cell function was evaluated by an intravenous glucose tolerance test. Results: Compared with NONLIPO and NAÏVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; >34%, P < 0.001), hepatic insulin sensitivity (>40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAÏVE, indicating an impaired adaptation of β-cell function to insulin resistance in LIPO. Conclusion: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and β-cell function.

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